Are Tonsils and Adenoids Secondary Reservoirs for Helicobacter pylori in Children? Why it Matters!!
|Abdullah M Nasrat1,*, Salwa AM Nasrat2, Randa M Nasrat3 and Mohammad M Nasrat3|
|1Department of Surgery, Balghsoon Clinic, Jeddah, KSA|
|2Department of Physical Therapy, Cardiac Surgery Academy, Cairo, Egypt|
|3Department of Internal Medicine, Helwan General Hospital, Helwan, Egypt|
|Corresponding Author :||Abdullah M Nasrat
Department of Surgery, Balghsoon Clinic
Jeddah, PO Box 5261 KSA-21573
Tel: +966 (012) 667 3645
E-mail: [email protected]
|Received: September 29, 2015 Accepted: October 19, 2015 Published: October 23, 2015|
|Citation: Nasrat AM, Nasrat SAM, Nasrat RM, Nasrat MM (2015) Are Tonsils and Adenoids Secondary Reservoirs for Helicobacter pylori in Children? Why it Matters!!. Gen Med (Los Angel) S1:006. doi:10.4172/2327-5146.1000S1-006|
|Copyright: © 2015 Nasrat AM, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.|
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The study aimed at demonstration of the possible existence of Helicobacter pylori in tonsils and adenoids and its possible risk sequences. The stomach wall represents the main and commonest habitat for H. pylori since an immemorial time; in a way indicating that mucosa of the stomach is the structure of the body that can recognize that stomach bacterium. Therefore; migration of H. pylori outside the stomach could encode autoimmunity. Tonsils and adenoids are lately discovered as secondary reservoirs for H. pylori in children. Further reports have confirmed the association of adenotonsillar hypertrophy with cytotoxin-associated gene A (cagA) positive H. pylori strains, and emphasized that cagA of H. pylori encodes high immunogenicity. Migration of H. pylori into the circulation could be an open gate for systemic complications; although H. pylori bacteremia is not a recognized behavior of a bacterium used to colonize the stomach, yet H. pylori bacteremia is clearly reported in literature. H. pylori can reside in dental plaques where it can feed on remnants of food in the mouth or bleeding from gums. Therefore; surgery on hypertrophied tonsils while migrating H. pylori strains exist around could attract these strains to gain feeding on the resulting oozing tonsil’s surgical bed with the possible potential risk and sequels of H. pylori bacteremia. 30 children aged 10-12 years with frank symptoms and family history of H. pylori dyspepsia scheduled for surgery because of hypertrophy of tonsils and adenoids were included in the study. They were divided into three equal groups; group 1 followed natural H. pylori eradication therapy and group 2 underwent surgery while group 3 followed antibiotic therapies before surgery. Existence of H. pylori strains was proved in children and parents by specific tests (urea breath test and H. pylori fecal antigen test).All children and parents were found positive for colonic H. pylori strains. Urea breath test was positive in most children. Adenoid/tonsil surgical specimens were mostly positive for H. pylori DNA. Regression of hypertrophy of tonsils was demonstrated in most children of the natural therapy first group and 7 of 10 children escaped surgery. On conclusion, existence of H. pylori should be ruled out and eliminated from the throat by natural measures before surgery of hypertrophied tonsils demonstrating no suppuration or inflammation.